Get Well Soon

At Wellness Garage, we believe that good health comes from good habits and behaviors.

Specifically there are six core behaviors that are the pillars of vibrant health - if any one of these pillars collapse, your general health will suffer:

Food

Activity

Sleep

Stress Response

Relationships

Purpose

It sounds so simple - master a set of habits for each behavior and you optimize your health.

So why does it feel so hard?

Two words explain it: Evolutionary Mismatch

Simply put - our evolutionary design did not prepare us for the modern world.

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Evolution through natural selection adapts organisms to their past environments and has no ability to foresee the future.

Across the six core behaviors:

Food - throughout human evolution food was scarce, times of abundance were followed by times of scarcity. Our bodies are designed to be able to store calories when food is abundant as fat, to be used in the future when food is once again scarce. Times of scarcity were also used by the body to clean up damaged cells and organelles and recycle proteins that have become dysfunctional. This clean-up processes called autophagy, is one of the keys for vibrant longevity. Our modern challenge lies in the challenge of over-nutrition, excess calories. Where fat storage is a one-way process and cellular clean-up never occurs.

Activity - humans were designed to move, to run, to walk, to climb and to lift. Evolution did not prepare us for desk jobs! Without exercise our bones and muscles become weak, resulting in the frailty associated with osteoporosis and sarcopenia.

Sleep - our bodies are designed a diurnal rhythm of light and dark. 30-40% of our genes are turned on or off by this rhythm. The 24/7 nature of our lifestyles with artificial light and our now ubiquitous screens from morning to night, distorts our bodies natural processes, disturbs our sleep and deprives us of the built in repair cycle that we are programmed to have every day.

Stress - this might be the most graphic mismatch. Evolution prepared us to respond to threats through our "fight or flight" response: our amygdala activates the HPA axis: the hypothalamus triggers the pituitary gland to release adrenocorticotropic hormone (ACTH) which then stimulates the adrenal glands to release adrenaline and cortisol into the bloodstream. This response is exactly what you need to mobilize your energy and blood supply to the large muscles that can either fight off the threat or run away from it. This makes sense when the threat is a tiger - not so much for an email or a rude driver! In our modern world, we trigger our HPA axis constantly - with the resulting stress affecting our health.

Relationships - humans evolved to live in relatively small groups where we all knew each other. It is estimated that our brains are limited in ability to maintain stable social relationships to approximately 150 people. This limit, also known as Dunbar's number, and is thought to be a direct function of the size of our neocortex. The average number of Facebook friends is 338, and 20% of users have more than 500. At the same time, familial relationships have broken down dramatically over the last 150 years. We no longer have long and stable relationships with multiple generations of our own families. Loneliness has become such a modern issue that the UK now has a minister of loneliness.

Purpose - for much of human existence our purpose was clear: to survive. With the advances of modern civilization and the taming of famine, pestilence and war - purpose is less clear. Traditionally, religion played a dominant role, but today many struggle with the notion of higher purpose.

Looked at this way - it is no wonder that the diseases of evolutionary mismatch are the chronic diseases that afflict us and imperil our vital longevity:

obesity

metabolic syndrome

diabetes

heart disease

cancer

dementia

osteoporosis

sarcopenia

and most auto-immune disease

At Wellness Garage, we believe that everyone needs a strategy to address these mismatches. ​Our programs systematically help people to find their own path to vibrant health by addressing the six core behaviors through the 18 principles we have outlined here.

The answer to evolutionary mismatch will be unique for each of us, but it will lie in our own behaviors.

​We are back - after a few weeks in South America: Galapagos and Machu Picchu!

​Our last post was about saturated fats and the back and forth controversy about the negative health effects (or not) from consuming saturated fat.

Many of you found this to be a bit deep in the weeds of science, so I thought this week's post would back up a little bit and provide an overview of fats with some take-home practical advice (and of course some science).

Let's start with definitions:

Fats - also known as triglycerides are esters of 3 fatty acid chains with glycerol serving as the backbone. Fat is one of the three main macronutrients, along with carbohydrates and proteins. Fats are broken down in the body to release glycerol (which is converted to glucose in the liver) and fatty acids. Each gram of fat releases 9 calories of energy. Fats are categorized according to the number and bonding of the carbon atoms:

Saturated fats have no double bonds between the carbons

Unsaturated fats have one or more double bonded carbons in the chain.

Polyunsaturated fats (PUFA) have multiple double bonds.

Monounsaturated fats (MUFA) have a single double bond. These are considered heart healthy.

Fatty acid chains may also differ by length, often categorized as short to very long:

Short-chain fatty acids (SCFA) are those with fewer than 6 carbons - they are produced by the good bacteria in your gut and provide the main source of nutrition for the cells in your colon. Their absorption into the blood also plays an important role in health - where they may reduce the risk for inflammatory diseases - including Type II Diabetes, heart disease, and obesity. More on this in the future.... How Short-Chain Fatty Acids Affect Health and Weight

Medium-chain fatty acids (MCFA) are those with 6–12 carbons, which can form medium-chain triglycerides (MCT's). MCT oil has some unique properties that can be leveraged to enhance fat metabolism and as part of a ketogenic strategy - again more on this in the future...

Long-chain fatty acids (LCFA) are those with 13 - 21 carbons

Very long chain fatty acids (VLCFA) areare those with 22 or more carbons.

Most fats (triglycerides) found in food, whether vegetable or animal, are made up of medium to long-chain fatty acids, usually of equal or nearly equal length.

For humans there are two essential fatty acids (fatty acids that we need for our health and cannot synthesize ourselves therefore we must consume in our diet), both are PUFA:

alpha linolenic acid (ALA) - an omega 3 fatty acid. (the 3 signifies that the double bond is three carbons in from the omega (or non-glycerol end). From ALA, we are able to synthesize the other important omega 3 fatty acids: eicosapentaenoic acid (EPA) and docosahexaenoic (DHA). The efficiency of this conversion is low (especially in the presence of high Omega 6’s) and is lower in men as compared to woman. There is also significant genetic variation with the FADS enzyme that converts ALA to DHA and EPA. As a result, it is generally recommended that EPA and DHA are obtained from diet (fish) and/or supplementation.

linoleic acid (LA) - an omega 6 fatty acid. (again the 6 means the double bond is six carbons in from the omega end).

(warning: we are diving back into the science)

Both Omega 3 and Omega 6 FA’s are important structural components of cell membranes, incorporated into phospholipids where they are affect membrane function. Increased dietary levels of Omega 3’s result increased membrane content of Omega 3’s with resulting improvement in membrane fluidity, flexibility, permeability and the activity of membrane-bound enzymes. DHA is selectively incorporated into retinal and neuronal membranes highlighting the important role it plays in vision and nervous system function.

It is worth noting that these membrane-bound HUFA are damaged by free radicals released by mitochondria under oxidative stress - this mechanism may be a contributing factor in the development of insulin resistance, the process whereby the membrane bound insulin receptor loses its ability to respond to insulin efficiently.

Under the influence of hormones and cytokines, membrane bound Omega 3 and Omega 6 FA’s are metabolized into multiple classes of PUFA-dervied bioactive lipids involved in inflammation and immune function.

Only ALA and LA are essential - all other Omega 6 and Omega 3 HUFA's can be derived from these precursors.

LA is common to many vegetable oils (corn, soybean, sunflower)ALA can be derived from plants sources - flax, chia seeds, green leafy vegetables, soybean oil, canola, and importantly from fish.

In general compounds derived from the Omega 6 pathway are inflammatory and those from the Omega 3 pathway are neutral, anti-inflammatory or even promote resolution of inflammation.

Evidence supports that increasing intakes of long chain Omega-3’s (EPA and DHA) decrease the risk of cardiac disease by:

preventing arrhythmias

decreasing the risk of thrombosis

decreasing serum triglycerides

slowing the growth of atherosclerotic plaques

improving vascular endothelial function

lowering blood pressure

decreasing inflammation

Studies show that long chain omega-3 FA’s (DHA in particular) have a protective effect in the development of Alzheimer’s Disease through

mitigation of inflammation

improved cerebral blood flow

reduced amyloid aggregation

Omega-3 and Omega-6 FA’s also modulate the expression of genes associated with fatty acid metabolism and inflammation by interacting with transcription factors.

Omega 3’s suppress NFkB a transcription factor associated with inflammation; as well as suppressing SREBP-1 which decreases fatty acid synthesis. In this way Omega-3 PUFA functions as feedback inhibitors of fatty acid synthesis.

There are two challenges to Omega 3 metabolism from ALA to EPA and DHA:

the enzymes to convert LA and ALA into their respective metabolites compete. In the presence of high levels of LA, ALA conversion to anti-inflammatory EPA and DHA will be very limited to non-existent. Historically humans consumed roughly equal amounts of Omega 3's to Omega 6. Now the ratio in Western diets is 25:1. At these levels, we cannot metabolized ALA to protective EPA or DHA.

the second problem is that overall efficiency of the conversion is low (lower in men than women) and there are significant common genetic variants in the FADS enzyme that further worsens the conversion.

So for all effects and purposes, we must consume EPA and DHA from our diet - if we want to ensure we want to get the Omega 3 health benefits.

EPA and DHA are most commonly consumed from cold water fish or fish oil. The actual compounds are synthesized by algae and are preserved in the food chain in fish oil, so it is possible to get algae derived EPA and DHA (important for vegans, and probably the most ecologically sustainable).

The key to getting the health benefits of the essential fatty acids is to get a proper balance of Omega 6 to Omega 3.

From an evolutionary perspective, the ratio of Omega 6 to Omega 3 in the diet was 1:1. Since the introduction of cheap, industrial vegetable oils - corn, soybean, safflower etc. into the Western diet - this ratio has sky-rocketed to 25:1. At these levels, Omega 6's act as pro-inflammatory agents and likely are a significant contributor to obesity, insulin resistance and heart disease.

These industrial oils are pervasive in packaged foods and restaurant prepared meals and should be avoided.

The easiest substitution is to use extra virgin olive oil or avocado oil instead. These oils are predominantly monounsaturated.

At the same time, increasing Omega 3's, either through the consumption of fish or through Omega 3 supplements.

Research suggest that an Omega 6 to Omega 3 ratio of 2:1 may guard against certain cancers, reduce inflammation in rheumatoid arthritis, and potentially decrease the risk of heart disease and Alzheimer's

The relative amount of EFA requirement is relatively small - about 1% of daily energy requirements from each of these two classes. 1% of 2000 calories = 20 calories - 9 calories per gm of fat = 2.2 g each of Omega 3 and Omega 6.

For more precision you can measure how much Omega 3's you need to consume by measuring one of two metrics:

Omega-3 index: is defined as the amount of EPA plus DHA in red blood cell membranes as expressed as the percent of total RBC membrane. High risk <4%; intermediate risk 4-8% and low risk >8%. Recommended dose of EPA to increase levels to >5% is 1 g/day, which is equivalent to 3 oz of salmon; however there is significant variation as some people need more to achieve these levels. Further individuals at higher risk benefit from higher levels of EPA+DHA. At Wellness Garage we can measure these levels for clients.

Blood EPA/AA ratio is also clinically relevant - high ratios have been associated with lower incidence of major coronary artery events - this ratio appears to account for most of the difference between Japenese and Americans in terms of heart disease.

Since the requirements for essential fats is small in both a relative and absolute sense, we come back to the question - what fats to eat?

One line of thinking when it comes to dietary fat, it to consume fat in the form that the body likes to store:

Composition of fat stored in adipose tissue:

55% = MUFA

18% = PUFA

27% = SFA

Interestingly a 50:50 mixture of butter and olive oil approximates the composition of triglycerides stored in our bodies.

But isn't Saturated Fat bad for you ? Probably not - see this blog post.

Current evidence does not support that dietary intake of saturated fat increases risk of CVD.

While increased levels of circulating SFA does correlate with increased risk of CVD and Diabetes - dietary intake of fat does not determine circulating SFA. In a fat adapted individual (someone who is burning fat for energy), dietary SFA will be quickly consumed as fuel. The real danger is the combination of high fat and high carbohydrate intake, where both dietary intake and insulin action will increase circulating SFA. What does get confusing is evidence that replacing saturated fat with PUFA improves CVD risk.